Abstract

The isolated chick retina provides an in vitro tissue model, in which two protocols were developed to verify the efficacy of a peptide in the excitability control of the central gray matter. In the first, extra-cellular potassium homeostasis is challenged at long intervals and in the second, a wave is trapped in a ring of tissue causing the system to be under self-sustained challenge. Within the neuropil, the extra-cellular potassium transient observed in the first protocol was affected from the initial rising phase to the final concentration at the end of the five-minute pulse. There was no change in the concomitants of excitation waves elicited by the extra-cellular rise of potassium. However, there was an increase on the elicited waves latency and/or a rise in the threshold potassium concentration for these waves to appear. In the second protocol, the wave concomitants and the propagation velocity were affected by the peptide. The results suggest a synergetic action of the peptide on glial and synaptic membranes: by accelerating the glial Na/KATPase and changing the kinetics of the glial potassium channels, with glia tending to accumulate KCl. At the same time, there is an increase in potassium currents through nerve terminals.

Highlights

  • The isolated chicken retina provides an experimental model that have been studied for more than 40 years and basic research on the spreading excitation phenomenon is well developed (Martins-Ferreira and Oliveira e Castro 1966, Martins-Ferreira and Do Carmo 1987, Fernandes de Lima and Hanke 1997)

  • Extra-cellular potassium homeostasis is challenged at long intervals and in the second, a wave is trapped in a ring of tissue causing the system to be under self-sustained challenge

  • The extra-cellular potassium transient observed in the first protocol was affected from the initial rising phase to the final concentration at the end of the five-minute pulse

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Summary

Introduction

The isolated chicken retina provides an experimental model that have been studied for more than 40 years and basic research on the spreading excitation phenomenon is well developed (Martins-Ferreira and Oliveira e Castro 1966, Martins-Ferreira and Do Carmo 1987, Fernandes de Lima and Hanke 1997). VERA M.F. DE LIMA, JOSÉ R.C. PIQUEIRA and WOLFGANG HANKE waves have been recorded in this experimental model (Ulmer et al 1995, Dahlem and Hanke 2005). One could predict the effects on the electrophysiological potassium wave concomitants (Do Carmo and MartinsFerreira 1984) recorded in the experiments reported in this paper. The expected results were: lower amplitude of the wave concomitants, acceleration of equilibrium within the neuropil of exogenous potassium pulses, rise in threshold for wave elicitation and decrease in propagation velocity of excitation waves (retinal spreading depression waves)

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